Faculty Opinions recommendation of Calcium balance in dialysis is best managed by adjusting dialysate calcium guided by kinetic modeling of the interrelationship between calcium intake, dose of vitamin D analogues and the dialysate calcium concentration.

Author(s):  
Daniel Schneditz ◽  
Peter Krisper
1997 ◽  
Vol 17 (6) ◽  
pp. 554-559 ◽  
Author(s):  
Susanne Bro ◽  
Lisbet Brandi ◽  
Henrik Daugaard ◽  
Klaus Olgaard

Objective To evaluate risk/benefit of various continuous ambulatory peritoneal dialysis (CAPD) dialysate calcium concentrations. Data Sources A review of the literature on the effects of various CAPD dialysate Ca concentrations on plasma Ca, plasma phosphate, plasma parathyroid hormone (PTH), doses of calcium carbonate, doses of vitamin D analogs, and requirements of aluminum-containing phosphate binders. Study Selection Eleven studies of nonselected CAPD patients, and 13 studies of CAPD patients with hypercalcemia were reviewed. Results In nonselected CAPD patients, treatment with a reduced dialysate Ca concentration (1.00, 1.25, or 1.35 mmol/L) improved the tolerance to calcium carbonate and/or vitamin D metabolites and reduced the need for Al-containing phosphate binders. When using dialysate Ca 1.25 or 1.35 mmol/L, the initial decrease of plasma Ca and increase of PTH could easily be reversed with an immediate adjustment of the treatment. After 3 months, stable plasma Ca and PTH levels could be maintained using only monthly investigations. In patients with hypercalcemia and elevated PTH levels, treatment with dialysate Ca concentrations below 1.25 mmol/L implied a considerable risk for the progression of secondary hyperparathyroidism. When hypercalcemia was present in combination with suppressed PTH levels, a controlled increase of PTH could be obtained with a temporary discontinuation of vitamin D and/or a reduction of calcium carbonate treatment in combination with a dialysate Ca concentration of 1.25 or 1.35 mmol/L. Conclusion Most CAPD patients can be treated effectively and safely with a reduced dialysate Ca concentration of 1.35 or 1.25 mmol/L. Treatment with dialysate Ca concentrations below 1.25 mmol/L should not be used. A small fraction of patients with persistent hypocalcemia need treatment with high dialysate Ca, such as 1.75 mmol/L.


1965 ◽  
Vol 209 (3) ◽  
pp. 637-642 ◽  
Author(s):  
William Y. W. Au ◽  
Lawrence G. Raisz

The effects of variations in vitamin D and calcium intake on parathyroid weight and amino acid uptake were studied in vivo. D-deficient rats on low or normal calcium intake developed hypocalcemia, parathyroid enlargement, and increased parathyroid uptake of α-aminoisobutyric acid (AIB). D-deficient rats fed a high-calcium diet and D-treated rats fed a normal-calcium diet had normal serum calcium concentrations, smaller parathyroids, and lower parathyroid uptake of AIB. When serum calcium concentration of vitamin D-deficient rats was increased acutely by vitamin D treatment, dietary lactose, or injection of calcium, parathyroid uptake of AIB decreased. Low-calcium medium stimulated and high-calcium medium suppressed AIB uptake of parathyroids from vitamin D-deficient rats in vitro. Parathyroids from vitamin D-deficient rats secreted bone-resorbing material in tissue cultures. The data indicate that both size and functional activity of rat parathyroids are inversely related to serum calcium concentration, and do not depend on the presence or absence of vitamin D.


Author(s):  
Rosilene M. Elias ◽  
Sharon Moe ◽  
Rosa M. A Moysés

Abstract Patients on hemodialysis are exposed to calcium via the dialysate at least three times a week. Changes in serum calcium vary according to calcium mass transfer during dialysis, which is dependent on the gradient between serum and dialysate calcium concentration (d[Ca]) and the skeleton turnover status that alters the ability of bone to incorporate calcium. Although underappreciated, the d[Ca] can potentially cause positive calcium balance that leads to systemic organ damage, including associations with mortality, myocardial dysfunction, hemodynamic tolerability, vascular calcification, and arrhythmias. The pathophysiology of these adverse effects includes serum calcium changes, parathyroid hormone suppression, and vascular calcification through indirect and direct effects. Some organs are more susceptible to alterations in calcium homeostasis. In this review, we discuss the existing data and potential mechanisms linking the d[Ca] to calcium balance with consequent dysfunction of the skeleton, myocardium, and arteries.


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